Contribution of heart muscle, liver, skeletal muscle and placenta to the asphyxial hypoxanthine elevation in the acutely exteriorised fetal lamb.

The metabolic response to different degrees of hypoxia was studied in 14 lamb fetuses. We have previously found a substantial rise in the fetal arterial plasma hypoxanthine (HX) level, in parallel with alterations of other hypoxia indices during induced asphyxia. Measurements of the arterio-venous (A-V) difference in the HX level across the CNS demonstrated a late efflux of this substance from the fetal brain, with a high resistance to asphyxia. In this study, the effluxes of HX, lactate, and in some cases glucose, from the myocardium, liver, hindleg (skeletal muscle) and placenta were investigated in acutely exteriorised sheep fetuses with graded asphyxia. The main findings were as follows: (a) myocardium: a release of HX early during asphyxia, the magnitude of which paralelled the amount of mechanical work performed by the heart; a significant lactate influx into the heart during normoxia and recovery period; (b) liver: hepatic HX release even during normoxia, increasing to substantial amounts in connection with increasing asphyxia; (c) hindleg: release of HX only during the recovery period; lactate efflux during all periods apart from severe asphyxia, when an influx was seen for both substances; (d) placenta: production of lactate during normoxia, and an efficient clearance of both lactate and HX from the fetal plasma in combination with their concentration increasing during asphyxia. It is concluded that the myocardium and liver are the main contributors to the elevated HX level during fetal asphyxia among the fetal organs investigated, while skeletal muscle releases HX mostly during the period of reoxygenation.